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二氧化碳对人体脑动脉直径无影响。

Lack of effect of CO2 on cerebral arterial diameter in man.

作者信息

Djurberg H G, Seed R F, Evans D A, Brohi F A, Pyper D L, Tjan G T, al Moutaery K R

机构信息

Department of Anesthesia, Armed Forces Hospital, Riyadh, Saudi Arabia.

出版信息

J Clin Anesth. 1998 Dec;10(8):646-51. doi: 10.1016/s0952-8180(98)00107-x.

Abstract

STUDY OBJECTIVE

To establish the quantitative effects on the diameter of cerebral arteries following controlled changes in arterial carbon dioxide tension (PaCO2).

DESIGN

Nonrandomized interventional study.

SETTING

Angiography suite of a tertiary referral hospital.

PATIENTS

12 anesthetized patients suffering from a cerebral arteriovenous malformation undergoing endovascular treatment.

INTERVENTION

Induced hypocapnia by hyperventilation and induced graded hypercapnia by the administration of carbon dioxide to the anesthetized patient's breathing circuit.

MEASUREMENTS AND MAIN RESULTS

A digital angiography computer was used to make computerized measurements and calculations of the diameter of deep and small cortical arteries outside the vascular territory of cerebral arteriovenous malformations following controlled and standardized changes in PaCO2. Cardiovascular parameters were simultaneously measured and cardiac output (CO) calculated. No statistically significant changes in the diameter of cerebral arteries down to a size of 0.57 mm, which was the smallest artery studied, could be observed following changes in PaCO2 in the range between 28 +/- 4 mmHg and 74 +/- 4 mmHg. However, there was a 64% change in cardiac index following the above change in PaCO2.

CONCLUSION

Deep cortical cerebral arteries down to a diameter of 0.57 mm seem to act merely as conductance vessels. The observed dramatic increase in CO following an increase in PaCO2 may offer an explanation for the changes in cerebral blood flow and cerebral flow velocity recorded by others and usually attributed to cerebral vasodilatation, which we were unable to demonstrate in this study.

摘要

研究目的

确定动脉二氧化碳分压(PaCO2)发生可控变化后对脑动脉直径的定量影响。

设计

非随机干预性研究。

地点

一家三级转诊医院的血管造影室。

患者

12例患有脑动静脉畸形并接受血管内治疗的麻醉患者。

干预措施

通过过度通气诱导低碳酸血症,通过向麻醉患者的呼吸回路中注入二氧化碳诱导分级高碳酸血症。

测量与主要结果

使用数字血管造影计算机对脑动静脉畸形血管区域外的深部和小皮质动脉直径进行计算机化测量和计算,测量在PaCO2发生可控且标准化变化之后。同时测量心血管参数并计算心输出量(CO)。在PaCO2在28±4 mmHg至74±4 mmHg范围内变化后,未观察到直径小至0.57 mm(所研究的最小动脉)的脑动脉直径有统计学上的显著变化。然而,在上述PaCO2变化后,心脏指数有64%的变化。

结论

直径小至0.57 mm的深部皮质脑动脉似乎仅起传导血管的作用。观察到的PaCO2升高后CO的显著增加,可能为其他人记录的脑血流量和脑血流速度变化提供了解释,这些变化通常归因于脑血管扩张,但在本研究中我们未能证实这一点。

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